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Clinical Biomedicine > W7: Bleeding Disorders > Flashcards

W7: Bleeding Disorders Flashcards

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1
Q

diff btwn primary + secondary haemostatic disorder

A

primary hemostasis = formation of primary platelet plug
secondary hemostasis = coagulation cascade/formation of blood clot

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2
Q

examples of PHD + SHD

A

PHD = thrombocytopenia
VWD

SHD = haemophilia

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3
Q

PHD vs SHD: bleeding

A

p - immediate
s - delayed

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4
Q

PHD vs SHD: petechiae

A

p - yes
s - no

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5
Q

PHD vs SHD: epistaxis

A

p - common
s - uncommon

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6
Q

PHD vs SHD: menorrhagia

A

p - common
s - uncommon

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7
Q

PHD vs SHD: Haemarthroses

A

p - no
s - yes

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8
Q

PHD vs SHD: intramuscular haematomas

A

p - uncommon
s - common

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9
Q

PHD vs SHD: gender

A

p - equal
s - >80% male

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10
Q

Bleeding defects may result from

A

leaky vessels
low platelet number (thrombocytopenia)
low platelet function
low coagulation

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11
Q

Thrombocytopenia - Causes

A

Failure of marrow production
Drug-induced
DIC
Sequestration - pooling of platelets in Splenomegaly
Massive blood transfusion-> dilution

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12
Q

define ITP - Idiopathic thrombocytopenic purpura (immune destruction)

A

Sudden onset of immunological destruction of platelets and thus thrombocytopenia.

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13
Q

ITP acute vs chronic

A

A
Sudden onset in children, often after illness.
90% spontaneous remission after few weeks

C
Gradual onset in adults (3F:1M) (no previous viral infection)
Autoantibodies (antibodies against self)
Platelets destroyed in spleen + liver (within a few hours).
usually lifelong condition

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14
Q

ITP diagnosis (A +C)

A

Low platelet no.
Large platelets
[Hb] + WBC typically normal
Tests for autoantibodies

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15
Q

ITP treatment (A vs C)

A

A - observation
C - Corticosteroids (supress immune sys)
Splenectomy
Immunosuppressive drugs
Platelet transfusions (short term benefit)
Stem cell transplantation

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16
Q

define TTP - Thrombotic thrombocytopenic purpura

A

Formation of vWF multimers -> platelet aggregation (thrombosis) -> thrombocytopenia

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17
Q

2 types of TTP + diff

A

acquired - Ab blocks protease that breaks down vWF multimers

inherited - protease absent/ defective

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18
Q

TTP diagnosis

A

thrombocytopenia
schistocytosis, (fragmented RBCs)
incr serum LDH
Coagulation NORMAL unlike in DIC.

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19
Q

TTP treatment

A

Plasma exchange
to remove vWF multimers + Ab + provide protease

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20
Q

what’s DIC
disseminated intravascular coagulation

A

Thrombosis + bleeding at the same time (in diff parts of body)

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21
Q

DIC usually happens when what other conditions also occurring

A

Infections - sepsis
Malignancy
Wide spread tissue damage (surgery / trauma / burns)
Anaphylaxis

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22
Q

DIC treatment depends on whether patient bleeding (treatment x) or thrombotic (treatment y)

Study These Flashcards
A

fresh frozen plasma
heparin

23
Q

steps of platelet plug formation

Study These Flashcards
A

adhesion
activation
aggregation

24
Q

disorders of platelet function
inherited vs acquired

Study These Flashcards
A

Inherited
Platelet adhesion defects
Activation defects
Secretion defects
Aggregation defects

Acquired
Aspirin and other drugs
Chronic renal failure
Cardiopulmonary bypass
Haematological diseases

25
what can vWF in plasma protein bind to on surface of platelets (2) + effect
collagen GPIb complex initial interaction not v strong so only slows platelet down
26
what's most common inherited bleeding disorder
VWD
27
3 types of VWD + what does it depend on
Type 1: Quantitative partial deficiency Type 2: Functional abnormality Type 3: Complete deficiency depends on autosomal recessive or dominant mutation
28
where is vWF prod (2) + roles (2)
endothelial cells + megakaryocytes roles platelet adhesion carries FVIII prolonging its half life
29
vWF gene is on chromosome
12
30
VWD diagnosis
Usually normal platelet number + morphology bleeding prolonged aPTT prolonged PT normal, TT normal vWF levels often low FVIII levels often low
31
VWD treatment
no treatment req Education - drug avoidance (aspirin), contact sport avoidance Genetic counselling Desmopressin - induces release of vWF from endothelium Tranexamic acid (antifibrinolytic)
32
what's Bernard-Soulier Syndrome
inherited: platelet adhesion defect GPIb complex
33
2 examples of inherited: activation defects
GPVI deficiency cyclooxygenase deficiency
34
examples of inherited: secretion defects
Grey platelet syndrome Platelets lack alpha granules ( so look grey) Wiskott-Aldrich Syndrome platelets (+ other cells) lack dense granules (+ are smaller) + thrombocytopenia
35
Example of inherited: Aggregation Defects
Glanzmann’s thrombasthenia integrin aIIbB3 defect Inability of platelets to bind fibrinogen + form platelet plug
36
Glanzmann’s thrombasthenia symptoms
Easy bruising menorrhagia
37
Glanzmann’s thrombasthenia diagnosis
normal platelet no. + morphology prolonged bleeding
38
Glanzmann’s thrombasthenia treatment
Education Local haemostatic agents (“quick clotters”) Platelet transfusions Genetic counselling
39
Acquired Platelet Disorders: Aspirin + other drugs
Anti-platelet drug Inhibits cyclooxygenase-1 decr in prod of thromboxane A2 (in platelets) decr prod of PGI2 (in endothelial cells)
40
Acquired Platelet Disorders: Aspirin + other drugs treatment
platelet transfusion desmopressin (induces release of vWF from endothelial cells)
41
Acquired Platelet Disorders: Chronic Renal Failure Renal failure causes incr bleeding time due to either
Uraemia (high nitrogen in blood leading to multiple platelet defects) Anaemia ( decr Epo synthesis by kidneys) Affects platelet – vessel wall interactions
42
Acquired Platelet Disorders: Chronic Renal Failure treatment
RBC packs (bulk blood, pushing platelets to the vessel walls) Platelet transfusions (limited effect as then in uraemic plasma)
43
Acquired Platelet Disorders: Cardiopulmonary bypass
Platelet activation and degranulation occurs in the extracorporeal circuit (out of the body).
44
Acquired Platelet Disorders: Cardiopulmonary bypass treatment
Platelet transfusion
45
Haematologial diseases: Several blood diseases impair platelet function
Most of the leukaemias (bone marrow activity affected). Myeloma (plasma B-cells ie bone marrow affected).
46
Reduced coagulation tends to arise from
A deficiency in a coagulation factor Inherited incl. fibrinogen Acquired
47
Inherited: Coagulation factor deficiencies Haemophilia A
Deficiency in FVIII. X-linked recessive disorder. Mostly inherited, though 30% due to sporadic mutations. Severity varies from mild to severe.
48
Inherited: Coagulation factor deficiencies VWD
vWF carries FVIII Most common inherited bleeding disorder 1:100 (asympt) 1:10 000 (sympt). Autosomal dominant/recessive.
49
Inherited: Coagulation factor deficiencies Haemophilia B
Deficiency in FIX. X-linked recessive disorder. Severity variable
50
other factor deficiencies - autosomal recessive
FXI FVII FV FXIII
51
Abnormalities of fibrinogen
Quantitative deficiencies Apofibrinogenaemia - Autosomal recessive. Severe symptoms. Hypofibrinogenaemia - Less defined. Milder symptoms. Qualitative deficiencies Dysfibrinogenaemia- Autosomal dominant. haemorrhagic effect (50%) thrombotic effect (10%)
52
Acquired: Coagulation factor deficiencies (3)
Liver Disease site of synthesis of several clotting factors (+ thrombopoietin) Liver function tests include: Albumin, Bilirubin, Prothrombin Time Vitamin K deficiency The reduced form of Vitamin K is needed for post-translational modification of several clotting factors (when synthesised). Warfarin use Warfarin inhibits the enzyme that cycles Vitamin K (vitamin K epoxide reductase
53
Acquired: Coagulation factor deficiencies Acquired haemophilia diagnosis +treatment
Generally neutralising autoantibody against FVIII Diagnosed with inhibitor assays Treatment: Human FVIII not effective Recombinant porcine FVIII better Immunosuppressive therapy

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